童建華

研究方向

長期從事有關白血病發病及治療分子機制的基礎研究，參加了血研所一系列重大的科研項目，在維甲酸誘導分化治療APL的基礎理論研究方面取得了可喜的成績。他主要針對髓系白血病細胞分化和凋亡過程中的信號轉導途徑以及相關基因的功能進行深入研究，曾在國際上率先報道了環腺苷酸具有參與介導As2O3誘導分化APL細胞的功能，為闡明As2O3誘導緩解治療APL的作用機制提供了依據。這些年來，童建華先後承擔了多項國家自然科學基金項目和國家科技部863計劃，並先後獲得了上海市科委啟明星計劃和上海市教委曙光計劃的資助。

代表性論文

1.Tong J-H（corresponding author）. Rig-G as a key mediator of the anti-proliferative activity of interferon-related pathways through enhancing p21 and p27 proteins. Proc. Natl. Acad. Sci. USA, 2006, in press

2.Tong J-H（corresponding author）. Rapid induction of cAMP/PKA pathway during retinoic acid-induced acute promyalocytic leukemia cell differentiation. Leukemia,2004, 18, 285-292

3.Tong J-H（corresponding author）. Synergic effects of arsenic trioxide and cAMP during acute promyelocytic leukemia cell maturation subtends a novel signaling cross-talk. Blood, 2002,99,1014-1022

4.Tong J-H (first author), Genomic organization of the JEM-1 (BLZF1) gene on human chromosome 1q24: Molecular cloning and analysis of its promoter region. Genomics, 2000, 69, 380-390.

5.Tong J-H (first author), Jem-1, a novel nuclear co-factor: localization and functional interaction with AP-1. Leukemia, 1999, 13, pp1982-1992.

6.Tong J-H (first author), Fant X, Duprez E, Benoit G, Uphoff C-C, Drexler H-G, Pla J-C, Lofvenberg E and Lanotte M.Expression patterns of the JEM-1 gene in normal and tumor cells:ubiquity contrasting with a faint, but retinoid-induced, mRNA expression in promyelocytic NB4 cells. Leukemia,1998,12,pp1733.

7.Tong J-H (co-first author), Cloning of a gene (RIG-G) associated with retinoic acid-induced differentiation of acute promyelocytic leukemia cells and representing a new member of a family of interferon-stimulated genes.Proc. Natl. Acad. Sci. USA, 1997, 94, 7406-7411

8.Tong J-H (co-first author), JEM-1, a novel gene encoding a leucine-zipper nuclear factor upregulated by retinoids during t(15;17) promyelocytic leukaemia maturation.Oncogene, 1997, 14, 1563-1570

9.Tong J-H (first author), Molecular rearrangements of the MYL gene in acute promyelocytic leukemia (APL, M3) define a breakpoint cluster region as well as some molecular variants. Oncogene, 1992, 7, 311